Modification of radiation-induced DNA double strand break repair pathways by chemicals extracted fromPodophyllum hexandrum: An in vitro study in human blood leukocytes

2014 ◽  
Vol 55 (5) ◽  
pp. 436-448 ◽  
Author(s):  
Nitya N. Srivastava ◽  
Sandeep K. Shukla ◽  
M.H. Yashavarddhan ◽  
Memita Devi ◽  
Rajendra P. Tripathi ◽  
...  
Keyword(s):  
Human Blood ◽  
In Vitro Study ◽  
Strand Break ◽  
Vitro Study ◽  
Double Strand Break Repair ◽  
Blood Leukocytes ◽  
Dna Double Strand Break ◽  
Radiation Induced ◽  
Repair Pathways

The PARP inhibitor olaparib induces significant killing of ATM-deficient lymphoid tumor cells in vitro and in vivo

Blood ◽  
2010 ◽  
Vol 116 (22) ◽  
pp. 4578-4587 ◽  
Author(s):  
Victoria J. Weston ◽  
Ceri E. Oldreive ◽  
Anna Skowronska ◽  
David G. Oscier ◽  
Guy Pratt ◽  
...  
Keyword(s):  
Cell Line ◽  
Tumor Cells ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Prolymphocytic Leukemia ◽  
Dna Double Strand Break ◽  
Break Repair

Abstract The Ataxia Telangiectasia Mutated (ATM) gene is frequently inactivated in lymphoid malignancies such as chronic lymphocytic leukemia (CLL), T-prolymphocytic leukemia (T-PLL), and mantle cell lymphoma (MCL) and is associated with defective apoptosis in response to alkylating agents and purine analogues. ATM mutant cells exhibit impaired DNA double strand break repair. Poly (ADP-ribose) polymerase (PARP) inhibition that imposes the requirement for DNA double strand break repair should selectively sensitize ATM-deficient tumor cells to killing. We investigated in vitro sensitivity to the poly (ADP-ribose) polymerase inhibitor olaparib (AZD2281) of 5 ATM mutant lymphoblastoid cell lines (LCL), an ATM mutant MCL cell line, an ATM knockdown PGA CLL cell line, and 9 ATM-deficient primary CLLs induced to cycle and observed differential killing compared with ATM wildtype counterparts. Pharmacologic inhibition of ATM and ATM knockdown confirmed the effect was ATM-dependent and mediated through mitotic catastrophe independently of apoptosis. A nonobese diabetic/severe combined immunodeficient (NOD/SCID) murine xenograft model of an ATM mutant MCL cell line demonstrated significantly reduced tumor load and an increased survival of animals after olaparib treatment in vivo. Addition of olaparib sensitized ATM null tumor cells to DNA-damaging agents. We suggest that olaparib would be an appropriate agent for treating refractory ATM mutant lymphoid tumors.

scholarly journals Mycobacteria exploit three genetically distinct DNA double-strand break repair pathways

2010 ◽  
Vol 79 (2) ◽  
pp. 316-330 ◽  
Author(s):  
Richa Gupta ◽  
Daniel Barkan ◽  
Gil Redelman-Sidi ◽  
Stewart Shuman ◽  
Michael S. Glickman
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dna Double Strand Break ◽  
Repair Pathways ◽  
Break Repair

Bamboo leaf extract ameliorates radiation induced genotoxicity: An in vitro study of chromosome aberration assay.

2021 ◽  
pp. 100528
Author(s):  
Shikha Tewari ◽  
Mansi Patel ◽  
Abhipsa VF Debnath ◽  
Priti Mehta ◽  
Snehal Patel ◽  
...  
Keyword(s):  
Chromosome Aberration ◽  
Leaf Extract ◽  
In Vitro Study ◽  
Vitro Study ◽  
Chromosome Aberration Assay ◽  
Radiation Induced

scholarly journals Resveratrol modulates DNA double-strand break repair pathways in an ATM/ATR–p53- and –Nbs1-dependent manner

2008 ◽  
Vol 29 (3) ◽  
pp. 519-527 ◽  
Author(s):  
Susanne Andrea Gatz ◽  
Marlen Keimling ◽  
Cindy Baumann ◽  
Thilo Dörk ◽  
Klaus-Michael Debatin ◽  
...  
Keyword(s):  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dependent Manner ◽  
Dna Double Strand Break ◽  
Repair Pathways ◽  
Break Repair
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